DNA repair mechanisms which have been identified in mitotically growing cells of the yeast Saccharomyces cerevisiae are being examined for their ability to protect cells undergoing meiosis from DNA-damaging agents. We have developed sucrose gradient techniques to examine repair in mitotic and meiotic cells after low doses of UV and ionizing radiation to wild-type and repair-defective strains. Using these techniques we are determining the role of mitotically identified repair functions on damage occurring during meiosis and correlating them with genetic events. There appears to be only one system for excision-repair throughout meiosis and that is controlled by the radl gene product. Cells can tolerate approximately 1500 pyrimidine dimers per cell during the early stages of meiosis due to an ability to synthesize DNA past dimers; as cells proceed through meiosis the damage has a greater lethal effect. These results are explained by bypass synthesis that is not associated with molecular recombination; on the contrary, the damage appears to depress recombination at the molecular and genetic levels. The observed loss in survival is probably due to effects on chromosomal disjunction resulting from loss in recombination.